Atherosclerosis is the principal contributor to the pathogenesis of myocardial and cerebral infarction, and no effective treatment is yet available for atherosclerosis. Identifying the etiological causes and understanding the pathogenic mechanisms of atherosclerosis may provide information for developing efficient strategies for preventing and/or controlling cardiovascular disease pathogenesis. Both epidemiological investigations and animal model studies have linked C. pneumoniae infection to atherosclerosis. The objectives of the present proposal are to further evaluate the role of C. pneumoniae infection in atherosclerosis in a mouse model system and to use this animal system to understand the mechanisms of C. pneumoniae atherogenesis by testing an infection / inflammatory response hypothesis. Specifically, the roles of both inflammatory responses and lipoprotein oxidation in C. pneumoniae exacerbation of atherosclerosis will be evaluated. These studies may provide the essential information on designing effective approaches for preventing and controlling C. pneumoniae-exacerbated atherosclerosis.